Abstract
Neurological disorders represent one of the most common disturbances accompanying HIV infection. In the past few years, highly antiretroviral active therapy has significantly reduced the incidence of HIV-related diseases. However, neurological dysfunction in AIDS patients still remains an unresolved problem. Oxidative stress, which occurs in brain tissues of patients undergoing HIV infection and is implicated in cell death of both astroglia and neurones, has recently been suggested to play a role in the pathogenesis of neuroAIDS. Thus, a better understanding of the processes that trigger and modulate free radical formation in brain tissues of AIDS patients might help in a successful therapeutic approach to the neuropathogenesis of HIV infection.
MeSH terms
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AIDS Dementia Complex / drug therapy
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AIDS Dementia Complex / metabolism*
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AIDS Dementia Complex / physiopathology
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Animals
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Anti-Inflammatory Agents, Non-Steroidal / pharmacology
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Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
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Antioxidants / metabolism*
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Astrocytes / drug effects
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Astrocytes / metabolism
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Blood-Brain Barrier / drug effects
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Blood-Brain Barrier / physiology*
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Catalase / metabolism
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Cell Death / drug effects
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Cell Death / physiology
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Free Radicals / metabolism*
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Gene Products, tat / metabolism
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Glutathione / metabolism
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HIV Infections / drug therapy
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HIV Infections / metabolism
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HIV Infections / physiopathology
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Humans
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Neurons / drug effects
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Neurons / metabolism
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Organometallic Compounds / pharmacology
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Organometallic Compounds / therapeutic use
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Oxidative Stress / drug effects
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Oxidative Stress / physiology*
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Superoxide Dismutase / metabolism
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tat Gene Products, Human Immunodeficiency Virus
Substances
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Anti-Inflammatory Agents, Non-Steroidal
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Antioxidants
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Free Radicals
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Gene Products, tat
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M40401
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Organometallic Compounds
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tat Gene Products, Human Immunodeficiency Virus
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Catalase
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Superoxide Dismutase
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Glutathione